Relay Therapeutics, Inc. · NASDAQ:RLAY
Relay Therapeutics — Investor Day (June 2024)
66 slides from Relay Therapeutics's investor day presentation, Jun 6, 2024
Slide 1: New Program & Platform Event June 2024
New Program & Platform Event June 2024 Exhibit 99.3
Slide 2: Disclaimer
Disclaimer This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, implied and express statements regarding the progress and timing of the clinical development of the programs across
Slide 3: Relay Tx – Today's Updates
Solid Tumors BREAST CANCER Relay Tx – Today’s Updates NRAS-Driven Solid tumors PI3Kα-Driven Breast Cancer 1 CDK4i clinical start by YE 2024 Clinical start in 2H 2025 ~150,000 pts1 ~28,000 pts4 1st PI3Kαi + ET + CDK4i combination in clinic 1st NRAS-selective inhibitor PI3Kα-Driven Vascular Malformati
Slide 4: PI3Kα – Large Opportunity Across Indications and Therapeutic Areas
PI3Kα – Large Opportunity Across Indications and Therapeutic Areas PIK3CA mutant HR+/HER2- Breast Cancer PIK3CA mutant Vascular Malformations PIK3CA mutant Other Solid Tumors Cerebral Cavernous Lymphatic Venous PROS 65k pt 65k pt 25k pt 15k pt ~150k Patients (US prevalence)1 ~170k Patients (US preva
Slide 5: Relay Tx – Productive Platform
Relay Tx – Productive Platform PEOPLE EXPERIMENTATION COMPUTATION PEOPLE Expected platform production by YE 2025 DCs 8 INDs 4 Clinical POC 2 Productive Platform Continued platform Productivity New clinical starts New DCs +3 New INDs +3 +3 ~$750M Cash as of end Q1 2024 Expected to fund current operat
Slide 6: Relay Tx's Dynamo – Productive Computationally Enabled Platform
2024 Dynamo™ Platform Relay Tx’s Dynamo™ – Productive Computationally Enabled Platform Free energy calculations Digitally encoded libraries Long time-scale MD Differential dynamics Automated Chemical Design Generative design Active learning ADME/PK models ML-DEL + AI models for DEL Giga-scale virtua
Slide 7: Focus of the Dynamo Platform
Focus of the Dynamo™ Platform Experimentation Develop novel modulation hypotheses Rapidly generate multiple lead compounds Optimize lead compounds swiftly and cost-effectively Development & Commercial Target Identification Target Modulation Hypothesis Hit Identification Lead Optimization Computation
Slide 8: Dynamo Platform Enabled Rapid Creation of First Selective NRAS Inhibitor
Dynamo™ Platform Enabled Rapid Creation of First Selective NRAS Inhibitor Compounds evaluated computationally In Vivo PoC 29 compounds synthesized in the lab 1st compound synthesized achieved potent NRAS inhibition 120 days
Slide 9: Relay Tx's Dynamo – Focused on Output
Outputs Relay Tx’s Dynamo™ – Focused on Output RLY-2608 RLY-5836 RLY-2139 RLY-1013 Migoprotafib Lirafugratinib COMPUTATION PEOPLE EXPERIMENTATION + Multiple unnamed earlier stage research programs Dynamo™ Platform
Slide 10: Consistent Focus on Validated, Low Translational Risk Programs
Relay Tx – Consistent Focus on Validated, Low Translational Risk Programs Breast Cancer Solid Tumors Genetic Disease Productive Dynamo™ Research Engine αGal (Fabry Disease) PI3Kα (Vascular Malformations) Multiple unnamed research stage programs New Programs Genetically Defined Clinically Validated U
Slide 11: Relay Tx – Broad Precision Medicine Pipeline
Relay Tx – Broad Precision Medicine Pipeline Target Program Preclinical Early Clinical Late Clinical BREAST CANCER PI3Kα RLY-2608 (PI3KαPAN) Endocrine Tx (ET) doublet Ribociclib + ET triplet CDK4i + ET triplet Other Novel Combinations CDK2 RLY-2139 ERα RLY-1013 (Degrader) GENETIC DISEASE Fabry Disea
Slide 12: Relay Tx – Milestones 2024-25
Relay Tx – Milestones 2024-25 Breast Cancer Portfolio Milestones RLY-1013 ERα PI3Kα RLY-2608 RLY-2139 CDK2 IND-ready in 2025 Data update in 4Q 2024 Doublet safety & efficacy data Initial triplet data CDK4i triplet clinic start by YE 2024 Potential pivotal trial start in 2025 IND-ready Genetic Diseas
Slide 13: PI3Kα – Large Opportunity Across Indications and Therapeutic Areas
PI3Kα – Large Opportunity Across Indications and Therapeutic Areas PIK3CA mutant HR+/HER2- Breast Cancer PIK3CA mutant Vascular Malformations PIK3CA mutant Other Solid Tumors Cerebral Cavernous Lymphatic Venous PROS 65k pt 65k pt 25k pt 15k pt ~150k Patients (US prevalence)1 ~170k Patients (US preva
Slide 14: Extensive Breast Cancer Portfolio in Validated Market
Relay Tx – Extensive Breast Cancer Portfolio in Validated Market Expected to Grow to ~$27B by 20301 …for which Relay Tx’s broad next generation ER+/HER2- BC Portfolio is designed to address HR+/HER2- Breast Cancer is a very large patient population… ~150k US prevalence HR+/HER2- Breast Cancer Patien
Slide 15: RLY-2608 + Atirmociclib: Pfizer Clinical Trial Collaboration
RLY-2608 + Atirmociclib (CDK4i): Pfizer – Relay Tx Clinical Trial Collaboration Potentially Differentiated Safety and Tolerability Profile Encouraging Efficacy Data in Heavily Pre-Treated Patients Source: Pfizer Oncology Innovation Day presentation, Feb 2024
Slide 16: RLY-2608 – Broad Development Program: Doublet
RLY-2608 – Broad Development Program: Doublet Mono Dose Escalation RLY-2608 + Fulvestrant Doublet RLY-2608 + Fulvestrant + CDKi Triplet Dose Expansion Ongoing ReDiscover Trial Initiated 2024 Completed (Started Apr 2022) 400mg BID (n=20) 600mg BID (n=60) Enrolling 600mg BID (N=17) 400mg BID (N=10) 20
Slide 17: RLY-2608 – Broad Development Program: Triplet
RLY-2608 – Broad Development Program: Triplet Mono Dose Escalation RLY-2608 + Fulvestrant Doublet RLY-2608 + Fulvestrant + CDKi Triplet Dose Expansion Ongoing ReDiscover Trial Completed (Started Apr 2022) 400mg BID (n=20) 600mg BID (n=60) Enrolling 600mg BID (N=17) 400mg BID (N=10) 20 pt enrolled be
Slide 18: RLY-2608 – Broad Development Program: Mono
RLY-2608 – Broad Development Program: Mono Dose Escalation RLY-2608 + Fulvestrant Doublet RLY-2608 + Fulvestrant + CDKi Triplet Dose Expansion ReDiscover Trial Completed (Started Apr 2022) Enrolling 600mg BID (N=17) 400mg BID (N=10) Enrolling Data Expectations for YE2024 Disclosure All Doses 600mg B
Slide 19: RLY-2608 – Broad Development Program
RLY-2608 – Broad Development Program Dose Escalation RLY-2608 + Fulvestrant Doublet RLY-2608 + Fulvestrant + CDKi Triplet Dose Expansion ReDiscover Trial Completed (Started Apr 2022) 400mg BID (n=20) 600mg BID (n=60) Enrolling 600mg BID (N=17) 400mg BID (N=10) 20 pt enrolled before YE 2023 Enrolling
Slide 20: Breast Cancer – Large Market in Current and Emerging Standards of Care
Breast Cancer – Large Market in Current and Emerging Standards of Care Endocrine Sensitive CDK4 + next gen oral ET Oral SERD monoTx Inavolisib + palbo + fulv Inavolisib + fulvestrant ADCs 11,000 pts Endocrine Resistant Capivasertib + fulvestrant or Alpelisib + fulvestrant or Everolimus + AI Elacestr
Slide 21: RLY-2608 – 2L PFS Pivotal Benchmark: ~6 Months
RLY-2608 – 2L PFS Pivotal Benchmark: ~6 Months 1. SABCS 2021 #P5-17-05; 2. Rugo 2021 Lancet Oncol 22:489, ASCO 2023 1078; 3. Turner N Engl J Med 2023; 388:2058-2070; 4. Based on 4.0-6.2mo mPFS reported in Novartis-sponsored real-world evidence study for alpelisib + fulvestrant (ASCO 2022 #1055); 5.
Slide 22: Relay Tx – Milestones 2024-25
Relay Tx – Milestones 2024-25 Breast Cancer Portfolio Milestones RLY-1013 ERα RLY-2139 CDK2 IND-ready in 2025 IND-ready Genetic Disease Portfolio milestones Solid Tumors portfolio milestones New Program NRAS Lirafugratinib FGFR2 Tumor agnostic data & regulatory update in 2H 2024 Migoprotafib SHP2 Th
Slide 23: Relay Tx – Today's Updates
CDK4i clinical start by YE 2024 ~28,000 pts4 ~170,000 pts2 (chronic treatment) Clinical start in 2H 2025 1st PI3Kαi + ET + CDK4i combination in clinic 1st NRAS-selective inhibitor Clinical start in 1Q 2025 1st mutant-selective PI3Kα inhibitor Clinical start in 2H 2025 1st non-inhibitory αGal chapero
Slide 24: PI3Kα-Driven Vascular Malformations – Significant Unmet Need
~170,000 patients1 (chronic treatment) Limited efficacy Lack of selectivity Approved Tx for PROS only Vijoice® (alpelisib) approved PIK3CAmut 1st mutant-selective PI3Kα inhibitor PI3Kα-Driven Vascular Malformations – Significant Unmet Need First Mutant Selective Inhibitor Dynamo™ Platform GENETIC DI
Slide 25: Dr. Adrienne Hammill, MD PhD
Dr. Adrienne Hammill, MD PhD 25 PhD in Cell Regulation “Asymmetric cell division results in differential apoptotic cell fates in a B-cell lymphoma model of tumor dormancy” Board certified in Pediatrics and Pediatric Hematology-Oncology Certificate in Clinical and Translational Research Working in va
Slide 26: Vascular Anomalies
Vascular Anomalies Dr. Adrienne Hammill, MD PhD 26 Anomalies is an umbrella term for many different diagnoses Includes TUMORS “things that grow” and MALFORMATIONS “present since birth” Distinction less clear than it used to be, a few “unclassified” Vascular Anomalies overall not rare due to high fre
Slide 27: Vascular Malformations
Vascular Malformations Dr. Adrienne Hammill, MD PhD 27 Vascular malformations can include a single type of malformed vessel, or combinations of vessels
Slide 28: Vascular Malformations
Vascular Malformations Dr. Adrienne Hammill, MD PhD 28 Vascular malformations can be localized (“isolated”), diffuse/multifocal, or part of a syndrome with other findings Most frequent syndromic association is overgrowth, particularly in “combined vascular malformations” A range of severity in Vascu
Slide 29: Genetic Causes of Vascular Malformations – Germline Mutations
Genetic Causes of Vascular Malformations – Germline Mutations Dr. Adrienne Hammill, MD PhD Key: Cell Membrane Receptor Tyrosine Kinases G-Protein Coupled Receptors PI3K AKT/PKB mTOR S6 eIF-4E Protein Synthesis VEGF Gα TIE2 RAS PTEN TSC1 TSC2 RASA1 PTEN-associated VAs/hamartomas TS-associated angiofi
Slide 30: Genetic Causes of Vascular Malformations – Somatic Mutations
Genetic Causes of Vascular Malformations – Somatic Mutations Dr. Adrienne Hammill, MD PhD Key: Cell Membrane Receptor Tyrosine Kinases G-Protein Coupled Receptors PI3K AKT/PKB mTOR S6 eIF-4E Protein Synthesis VEGF Gα TIE2 RAS PTEN TSC1 TSC2 RASA1 VMCM, BRBNS, sporadic VMs Sturge-Weber syndrome, CM (
Slide 31: Genetic Causes of Vascular Malformations
Genetic Causes of Vascular Malformations Dr. Adrienne Hammill, MD PhD Key: Cell Membrane Receptor Tyrosine Kinases G-Protein Coupled Receptors PI3K AKT/PKB mTOR S6 eIF-4E Protein Synthesis VEGF Gα TIE2 RAS PTEN TSC1 TSC2 RASA1 VMCM, BRBNS, sporadic VMs PTEN-associated VAs/hamartomas TS-associated an
Slide 32: PIK3CA-related Overgrowth Spectrum (PROS) Phenotypes
PIK3CA-related Overgrowth Spectrum (PROS) Phenotypes Sources: Mirzaa G et al. PIK3CA-Related Overgrowth Spectrum. 2013 Aug 15 [Updated 2023 Apr 6]. In: GeneReviews® [Internet] Megalencephaly-capillary malformation (MCAP) syndrome Dysplastic megalencephaly (DMEG), hemimegalencephaly (HMEG) and focal
Slide 33: PI3Kα-Driven Vascular Malformations – Overview of Biology
PI3Kα-Driven Vascular Malformations – Overview of Biology ~300k US patients affected by Vascular Malformations, driven by prenatal somatic mutations Abnormal development of lymphatic and/or blood vessels leads to a wide range of symptoms Malformations may involve one or more types of vasculature Mut
Slide 34: PI3Kα-Driven Vascular Malformations – Patient Treatment Journey
PI3Kα-Driven Vascular Malformations – Patient Treatment Journey Symptom Presentation Diagnosis Treatment PCP, Dermatologist, Surgeon, ENT, etc. Geneticist, “Vascular Anomalist” Surgeon, Int. Radiologist, Dermatologist, Heme-Onc Watch and wait; Compression Therapy Local Treatment: Laser, sclerotherap
Slide 35: PI3Kα-Driven Vascular Malformations – Over 170,000 US Patients
PI3Kα-Driven Vascular Malformations – Over 170,000 US Patients US Patients % PIK3CAmut Approved Therapies Lymphatic Malformation (LM) Venous Malformation (VM) Cerebral Cavernous Malformation (CCM) PIK3CA-Related Overgrowth Spectrum (PROS) ~80k 80% ~65k pt ~100k ~20-25% ~20-25k pt ~120k 40-55% ~50-65
Slide 36: Systemic Tx Limited by Non-Selective SoC
Non-Selective Limited scope, approved in PROS only Not approved in any Vascular Malformation types Non-Selective Immunosuppressive Alpelisib Lymphatic Malformations (LM) Venous Malformations (VM) Cerebral Cavernous Malformations (CCM) PIK3CA-Related Overgrowth Spectrum (PROS) PI3Kα-Driven Vascular M
Slide 37: Relay Tx Mutant Selective Approach
Favorable Selectivity Favorable Tolerability Favorable Efficacy PI3Kα-Driven Vascular Malformations – Relay Tx Mutant Selective Approach Selective for mutant PI3Kα Fewer key common PI3K class AEs* Reduction of mutant PIK3CA ctDNA* 6% 10% 59% 60% 29% RLY-26081 Alpelisib2 *interim data from oncology t
Slide 38: PI3Kα – Dynamo: Integration of Experimental and Computational Tools
PI3Kα – Dynamo™: Integration of Experimental and Computational Tools Discovery of 1st mutant-selective PI3Kα inhibitor Target Modulation Hypothesis Hit Identification Lead Optimization CryoEM & X-ray Crystallography Long Time-scale MD DNA-Encoded Libraries (DEL) Differential Dynamics Integrated Phar
Slide 39: PI3Kα-Driven Vascular Malformations – Significant Unmet Need
~170,000 patients1 (chronic treatment) Limited efficacy Lack of selectivity Approved Tx for PROS only Vijoice® (alpelisib) approved PIK3CAmut 1st mutant-selective PI3Kα inhibitor Clinical Start in Q1 2025 PI3Kα-Driven Vascular Malformations – Significant Unmet Need GENETIC DISEASE PI3Kα-Driven Vascu
Slide 40: Relay Tx – Today's Updates
CDK4i clinical start by YE 2024 ~28,000 pts4 ~150,000 pts1 ~170,000 pts2 (chronic treatment) ~8,000 pts3 (chronic treatment) Clinical start in 2H 2025 1st PI3Kαi + ET + CDK4i combination in clinic 1st NRAS-selective inhibitor Clinical start in 1Q 2025 1st mutant-selective PI3Kα inhibitor Clinical st
Slide 41: Fabry Disease – Large Validated Market With Significant Unmet Need
~8,000 patients1 (chronic treatment) Limited αGal activation & limited mutational coverage Galafold® (migalastat) approved in Fabry Disease GLA mutations 1st non-inhibitory αGal chaperone Fabry Disease – Large Validated Market With Significant Unmet Need First Non-Inhibitory αGal Chaperone Genetical
Slide 42: Fabry Disease – Large Validated Market With Significant Unmet Need
~$1.6B peak sales1 Fabry Disease – Large Validated Market With Significant Unmet Need Over 1,000 different GLA gene mutations Reduces αGal protein levels Leads to accumulation of toxic Gb3 substrate Broad clinical manifestations; Life threatening cardiac & renal disfunction Fabry disease is a lysoso
Slide 43: Dynamo Discovered a Novel Allosteric Pocket
αGal Inhibitory vs Non-Inhibitory Chaperone Normal Mutant Fabry Disease – Dynamo™ Discovered a Novel Allosteric Pocket Active Site
Slide 44: Fabry Disease – Dynamo: Integration of Experimental and Computational Tools
Fabry Disease – Dynamo™: Integration of Experimental and Computational Tools Discovery of 1st non-inhibitory αGal chaperone Discovered & validated novel allosteric pocket Identified & validated initial hits that stabilized Achieved potent αGal non-inhibitory chaperones 1 2 3 Computational tool Exper
Slide 45: Relay Tx Compounds are Non-Inhibitory Chaperones
Fabry Disease – Relay Tx Compounds are Non-Inhibitory Chaperones Migalastat inhibited αGal function while Relay Tx compounds did not Note: Biochemical assay run with WT αGal; 1 hr incubation at room temperature
Slide 46: Potential Benefits of Non-Inhibitory Chaperone Approach
Fabry Disease – Potential Benefits of Non-Inhibitory Chaperone Approach Superior αGal activation1 Broad mutational coverage2 Combinable with ERT3 1 2 3 Relay Tx Solution: Non-Inhibitory Chaperone to Stabilize Protein and Increase Activity Notes: 1. R301Q mut αGal (2hr post compound washout, expresse
Slide 47: Superior αGal Activation
There were no adverse findings in an exploratory rat toxicology study of RTX-1 at exposures equivalent to 100 mg/kg BID Superior αGal Activation 1 Relay Tx Non-Inhibitory Chaperones Can Lead to Higher Levels of In Vivo Activity
Slide 48: Broad Mutational Coverage
Relay Tx Non-Inhibitory Chaperones Have Broad Mutational Coverage In vitro αGal activity assay (4MU) across multiple GLA mutations expressed in HEK293 GLA KO cells Amenable | Non-Amenable (as per migalastat label) Broad Mutational Coverage 2 Note: αGal activity evaluated at 1uM of migalastat and RTX
Slide 49: Combinable with ERT
Relay Tx Non-Inhibitory Chaperones Combinable with ERT Combinable with ERT 3
Slide 50: Fabry Disease – Large Validated Market With Significant Unmet Need
~8,000 patients1 (chronic treatment) Limited αGal activation & limited mutational coverage Galafold® (migalastat) approved in Fabry Disease GLA mutations 1st non-inhibitory αGal chaperone Fabry Disease – Large Validated Market With Significant Unmet Need Genetically Defined Clinically Validated Unme
Slide 51: Relay Tx – Today's Updates
CDK4i clinical start by YE 2024 ~150,000 pts1 ~28,000 pts4 ~170,000 pts2 (chronic treatment) ~8,000 pts3 (chronic treatment) Clinical start in 2H 2025 1st PI3Kαi + ET + CDK4i combination in clinic 1st NRAS-selective inhibitor Clinical start in 1Q 2025 1st mutant-selective PI3Kα inhibitor Clinical st
Slide 52: NRAS – Large Validated Market With Significant Unmet Need
~28,000 patients1 Lack of selectivity Challenging AE profile Limited efficacy Non-selective RAF/MEK/Pan-RAS NRASmut 1st NRAS-selective inhibitor NRAS – Large Validated Market With Significant Unmet Need First NRAS Selective Inhibitor Dynamo™ Platform Solid Tumors NRAS-Driven Solid Tumors Genetically
Slide 53: NRAS – Large Validated Market With Significant Unmet Need
NRAS – Large Validated Market With Significant Unmet Need NRAS mutations observed in broad range of tumor types NRAS mutations are a key driver of solid tumors, though no NRAS-selective agent exists Head and Neck NSCLC Melanoma2 X ~0.6k ~2.2k ~4.0k ~0.4k ~6.4k ~1.1k Pancreatic Cancer Colorectal (CRC
Slide 54: Limited Therapeutic Window of Current Agents
based MEK + RAFi Pan-RAS Limited Therapeutic Window of Current Agents – Pan-RAF/RAS & MEK Inhibitors Limited Efficacy Limited Tolerability MEK + RAFi Pan-RAS Rash Liver Tox 25-80% <10-60% 81% 7-8% Limited Target Inhibition Dose Red. Dose Discont. 16-70% 7-28% 8% 1% High rates of skin toxicity driven
Slide 55: NRAS – Dynamo Platform Discovered a Novel Allosteric Pocket
NRAS – Dynamo™ Platform Discovered a Novel Allosteric Pocket Exploited differences in protein motion… …to design first NRAS-selective inhibitor NRAS HRAS KRAS NRAS HRAS KRAS
Slide 56: NRAS – Dynamo: Integration of Experimental and Computational Tools
NRAS – Dynamo™: Integration of Experimental and Computational Tools Discovery of 1st NRAS-selective inhibitor Discovered a novel cryptic pocket Identified & validated hits selective for NRAS (over H/KRAS) Rapidly designed & prioritized NRAS inhibitors 1 2 3 Target Modulation Hypothesis Hit Identific
Slide 57: NRAS Inhibitors Are Potent, Selective & Active Across NRAS Mutations
NRAS Inhibitors Are Potent, Selective & Active Across NRAS Mutations 1. Based on SPR analysis of purified protein; 2. Based on pERK assay of SK-MEL-2, SK-MEL-30, and CALU-6 cell lines evaluated at 24hr timepoint; 3. Based on cell proliferation panel (17 cell lines) evaluated at 3-5d timepoint depend
Slide 58: NRAS Inhibitors Achieve Complete Regression at Well Tolerated Doses
*Regressions also achieved with additional NRAS mutant models (NRAS Q61K and NRAS Q61R) NRAS Inhibitors Achieve Complete Regression at Well Tolerated Doses There were no adverse findings in an exploratory rat toxicology study of RTX-2 at exposures equivalent to 100mg/kg QD
Slide 59: NRAS – Large Validated Market With Significant Unmet Need
~28,000 patients1 Lack of selectivity Challenging AE profile Limited efficacy Non-selective RAF/MEK/Pan-RAS NRASmut 1st NRAS-selective inhibitor NRAS – Large Validated Market With Significant Unmet Need Solid Tumors NRAS-Driven Solid Tumors Genetically Defined Clinically Validated Unmet Medical Need
Slide 60: Relay Tx – Today's Updates
Solid Tumors BREAST CANCER Relay Tx – Today’s Updates NRAS-Driven Solid tumors PI3Kα-Driven Breast Cancer 1 4 CDK4i clinical start by YE 2024 Clinical start in 2H 2025 ~150,000 pts1 ~28,000 pts4 1st PI3Kαi + ET + CDK4i combination in clinic 1st NRAS-selective inhibitor PI3Kα-Driven Vascular Malforma
Slide 61: PI3Kα – Large Opportunity Across Indications and Therapeutic Areas
PI3Kα – Large Opportunity Across Indications and Therapeutic Areas PIK3CA mutant HR+/HER2- Breast Cancer PIK3CA mutant Vascular Malformations PIK3CA mutant Other Solid Tumors Cerebral Cavernous Lymphatic Venous PROS 65k pt 65k pt 25k pt 15k pt ~150k Patients (US prevalence)1 ~170k Patients (US preva
Slide 62: Dynamo – Internalizing Bespoke Tools In-House
Relay Tx Dynamo™ – Internalizing Bespoke Tools In-House Molecular Dynamics (MD) In-House REL-DEL In-House High-Throughput Automated Chemistry Dynamo™ Platform Development & Commercial Target Identification Target Modulation Hypothesis Hit Identification Lead Optimization
Slide 63: Dynamo – Continuing to Focus, Build and Evolve
Free energy calculations Digitally encoded libraries Long time-scale MD Differential dynamics Automated Chemical Design Generative design Active learning ADME/PK models ML-DEL + AI models for DEL Giga-scale virtual screening Computational fragment merging COMPUTATION EXPERIMENTATION Relay Tx Dynamo™
Slide 64: Relay Tx – Broad Precision Medicine Pipeline
Relay Tx – Broad Precision Medicine Pipeline Target Program Preclinical Early Clinical Late Clinical BREAST CANCER PI3Kα RLY-2608 (PI3KαPAN) Endocrine Tx (ET) doublet Ribociclib + ET triplet CDK4i + ET triplet Other Novel Combinations CDK2 RLY-2139 ERα RLY-1013 (Degrader) GENETIC DISEASE Fabry Disea
Slide 65: Relay Tx – Milestones 2024-25
Relay Tx – Milestones 2024-25 Breast Cancer Portfolio Milestones RLY-1013 ERα PI3Kα RLY-2608 RLY-2139 CDK2 IND-ready in 2025 Data update in 4Q 2024 Doublet safety & efficacy data Initial triplet data CDK4i triplet clinic start by YE 2024 Potential pivotal trial start in 2025 IND-ready Genetic Diseas
Slide 66: Slide 66